Format

Send to

Choose Destination
See comment in PubMed Commons below
Cancer Cell. 2009 Jun 2;15(6):477-88. doi: 10.1016/j.ccr.2009.04.002.

Modeling inducible human tissue neoplasia identifies an extracellular matrix interaction network involved in cancer progression.

Author information

1
Veterans Affairs Palo Alto Healthcare System, Palo Alto, CA 94306, USA. telse@umich.edu

Abstract

To elucidate mechanisms of cancer progression, we generated inducible human neoplasia in three-dimensionally intact epithelial tissue. Gene expression profiling of both epithelia and stroma at specific time points during tumor progression revealed sequential enrichment of genes mediating discrete biologic functions in each tissue compartment. A core cancer progression signature was distilled using the increased signaling specificity of downstream oncogene effectors and subjected to network modeling. Network topology predicted that tumor development depends on specific extracellular matrix-interacting network hubs. Blockade of one such hub, the beta1 integrin subunit, disrupted network gene expression and attenuated tumorigenesis in vivo. Thus, integrating network modeling and temporal gene expression analysis of inducible human neoplasia provides an approach to prioritize and characterize genes functioning in cancer progression.

PMID:
19477427
PMCID:
PMC3050547
DOI:
10.1016/j.ccr.2009.04.002
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center